Official food rations were below 1000 calories (4200 J) per person per day from January through April 1945. Pregnant women were allocated some additional food rations, but the extent to which redistribution of these additional rations occurred within families is not known. The famine ceased immediately with liberation in May 1945, when Allied food supplies became abundant.
This explanation highlights the importance of maternal vitality, (a synthetic, historically variable and culturally determined phenomenon) as a neglected feature of historical demography."
Ravelli et al conclude that prenatal exposure to famine, especially during late gestation, is linked to decreased glucose tolerance in adults.
A study hypothesized that if prenatal caloric restriction due to nutritional deprivation had affected development of the organs responsible for producing and regulating female reproductive hormones, a woman's fertility would be impaired. Acute famine exposure in utero appears to have no adverse consequences for a woman's fertility.
We hypothesized that if prenatal caloric restriction due to nutritional deprivation had affected development of the organs responsible for producing and regulating female reproductive hormones, a woman's fertility would be impaired.
Women born in Amsterdam from August 1, 1944, through April 15, 1946, a period encompassing a severe 5-month famine, were identified (n = 700; 85% response rate). Date of birth and vital status of all offspring were aed by home interview between 1987 and 1991. Famine exposure was inferred from the mother's date of birth.
Of the study participants, 74 (10.6%) had no children. The remainder reported 1334 offspring (1294 singletons, 20 pairs of twins), of whom 14 were stillborn and 22 died in the first 7 days of life. There was no detectable effect of famine exposure on age at menarche, the proportion having no children, age at first delivery, or family size. An excess of perinatal deaths occurred among offspring of famine exposed women, particularly those exposed in their third trimester.
Acute famine exposure in utero appears to have no adverse consequences for a woman's fertility. The excess perinatal mortality in the second generation is unexplained and should be confirmed by other studies.
Dutch men born in 1994-1946 who were given psychiatric examinations for military induction at age 18 were studied in terms of their prenatal exposure to nutritional deficiency to determine what correlation might exist between antisocial personality disorder (ASPD) and prenatal nutritional deficiency. The results are presented.
In a study, data from the Dutch Famine Birth Cohort Study were analyzed to determine the influence of acute famine on the relation of maternal weight gain to birth weight, length and ponderal index.
Infant survival is directly related to birth weight. Our data suggest cumulative
effects of severe nutritional deprivation during pregnancy on birth size, which may
be trimester specific. When weight gain is adequate, there is no relation between
weight gain and birth size. Once weight gain drops below 0.5 kg/week, however,
further reductions in weight gain are accompanied by reduced birth weight, length,
and ponderal index. Our exploratory analysis by cohort of exposure suggests that
the effects of famine on the relation between weight gain and birth size are trimester
specific, but this analysis is limited by the small sample sizes of the exposed
It is not clear whether famine-induced reduced length and ponderal index at birth
are maintained throughout life if food supplies are not restricted in childhood.
Preliminary data from follow-up of survivors of the present cohort show
persistence of the period effects on weight (but not height) through age 18 years
(Lumey et al. 1992). Among males subjected to in utero famine exposure and
examined at age 18 years, mid-pregnancy exposure was associated with reduced
body mass index, whereas an increased prevalence of obesity was observed among
males exposed in the first trimester (Ravelli et al. 1976). These data, although
population based, are limited to survivors, and birth length and weight data were not
available. Differential survival may be an important intermediate factor; among
births in our series (including those excluded from the present analysis) perinatal
and infant mortality exceeded 12% and mean birth weight was 500 g lower among
nonsurvivors than among survivors (Lumey et al. 1993).
In conclusion, nutritional deprivation severe enough to result in maternal weight loss or reduced weight gain results in a corresponding reduction in offspring length and ponderal index (and hence also birth weight). The relationship between maternal weight gain and infant birth size also holds in the nonfamine situation when weight gain is low. However, when weight gain is high (over 0.5 kg/week in this data set), no further increments in offspring birth size were observed with additional maternal weight gain. Our results affirm the hypothesis proposed by Susser (1991) that maternal nutritional deprivation affects fetal growth only below a threshold and that, conversely, even after a famine period offspring birth size does not respond in a linear fashion to ad libitum maternal feeding during the rehabilitation period. Further research is required to identify more precisely key periods of risk for the fetus.
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Institute of Medicine. 1990. Nutrition during Pregnancy, Part 1, Weight Gain. Washington, DC: National Academy Press.
Kramer, M.S., M. Olivier, F.H. McLean et al. 1990. Determinants of fetal growth and body proportionality. Pediatrics 86:18-26.
Lawton, F.G., G.C. Mason, K.A. Kelly et al. 1988. Poor maternal weight gain between 28 and 32 weeks gestation may predict small-for-gestational-age infants.Br. J. Obstet. Gynecol. 95:884-887.
Lumey, L.H., A.C.J. Ravelli, L.G. Wiessing et al. 1993. The Dutch Famine Birth Cohort Study: Design, validation of exposure, and selected characteristics of subjects after 43 years follow-up. Pediatr. Perinatal Epidemiol. 7:354-367.
Lumey, L.H., G.A. Stam, A.C.J. Ravelli et al. 1992. Birth weight, birth cohort, and adult weight among women born during the Dutch famine of 1944-45. Am. J Epidemiol. 136:951-952.
Miller, H.C., K. Hassanein, and P.A. Hensleigh. 1976. Fetal growth retardation in relation to maternal smoking and weight gain in pregnancy. Am. J. Obstet. Gynecol.125:55-60.
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Pebley, A.R., S.L. Huffman, A.K.M.A. Chowdhury et al. 1985. Intrauterine mortality and maternal nutritional status in rural Bangladesh. Popul. Stud. 39:425-440.
Ravelli, G., Z.A. Stein, and M.W. Susser. 1976. Obesity in young men after famine exposure in utero and early infancy. New Engl. J. Med. 295:349-353.
Sindram, I.S. 1953. De involved van ondervoeding op de groei van de vrucht [The influence of undernutrition on the growth of the fetus]. Ned. Tijdschr. Verloskde. Gynecol. 45:30-48.
Smith, C.A. 1947. Effects of wartime starvation in Holland on pregnancy and its products. Am. J. Obstet. Gynecol. 53:599-608.
Stein, Z., M. Susser, G. Saenger et al. 1975. Famine and Human Development: The Dutch Hunger Winter of 1944/45. New York: Oxford University Press.
Susser, M. 1991. Maternal weight gain, infant birthweight, and diet: Causal sequences. Am. J. Clin. Nutr. 53:1384-1396.
Trienekens, G.M.T. 1985. Tussens ons volk en de honger. De voedselvoorziening 1940-1945 [Between our people and the famine: The food distribution system,1940-1945]. Utrecht, Netherlands: Matrijs.
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6. Timing in prenatal nutrition: A reprise of the Dutch famine
Nutrition Reviews, v. 52, Iss. 3, p. 84- (Mar 1994).
Interest in prenatal nutrition as a subject of serious scientific study has fluctuated during the past 100 years. The study of the Dutch famine of 1944-45 is examined to illustrate the point that the effects of prenatal nutrition are obscured if the nutritional exposure is not closely defined in terms of developmental timing.
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"Other findings of the Dutch study show that the children of women who
were pregnant during the famine are more likely to develop late-onset
diabetes, resulting in an imbalance of blood sugars."